Mathematical models predict that the future of the multidrug-resistant tuberculosis epidemic will depend on the fitness cost of drug resistance. We show that in laboratory-derived mutants of Mycobacterium tuberculosis, rifampin resistance is universally associated with a competitive fitness cost and that this cost is determined by the specific resistance mutation and strain genetic background. In contrast, we demonstrate that prolonged patient treatment can result in multidrug-resistant strains with no fitness defect and that strains with low- or no-cost resistance mutations are also the most frequent among clinical isolates.

(I added the italics and bold type for emphasis. Note: no fitness defects in multi-drug resistant clinical isolates. That means they don't grow any slower, etc.)

Received 4 March 2005; returned 27 April 2005; revised 3 June 2005; accepted 23 June 2005

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* Corresponding author. Tel: +44-117-9287522; Fax: +44-117-9287896; E-mail: v.i.enne@bristol.ac.uk
Objectives: Little is known of the fitness cost that antibiotic resistance exerts on wild-type bacteria, especially in their natural environments. We therefore examined the fitness costs that several antibiotic resistance elements imposed on a wild-type Escherichia coli isolate, both in the laboratory and in a pig gut colonization model.

Methods: Plasmid R46, Tn1 and Tn7 and a K42R RpsL substitution were separately introduced into E. coli 345-2 RifC, a rifampicin-resistant derivative of a recent porcine isolate. The insertion site of Tn1 was determined by DNA sequencing. The fitness cost of each resistance element was assessed in vitro by pairwise growth competition and in vivo by regularly monitoring the recovery of strains from faeces for 21 days following oral inoculation of organic piglets. Each derivative of 345-2 RifC carrying a resistance element was grown in antibiotic-free broth for 200 generations and the experiments to assess fitness were repeated.

Results: RpsL K42R was found to impose a small fitness cost on E. coli 345-2 RifC in vitro but did not compromise survival in vivo. R46 imposed a cost both before and after laboratory passage in vitro, but only the pre-passage strain was at a disadvantage in vivo. The post-passage isolate had an advantage in pigs. Acquisition of Tn7 had no impact on the fitness of E. coli 345-2 RifC. Two derivatives containing Tn1 were isolated and, in both cases, the transposon inserted into the same cryptic chromosomal sequence. Acquisition of Tn1 improved fitness of E. coli 345-2 RifC in vitro and in vivo in the case of the first derivative, but in the case of a second, independent derivative, Tn1 had a neutral effect on fitness.

Conclusions: The fitness impact imposed on E. coli 345-2 RifC by carriage of antibiotic resistance elements was generally low or non-existent, suggesting that once established, resistance may be difficult to eliminate through reduction in prescribing alone.

(I added the bold type for emphasis. Resistant strains may be at a disadvantage in the lab, but not in the host animal or human. Also note that the paper says it may be difficult to get rid of the resistant strains once they are established, so contrary to what you might believe, they aren't reverting quickly to non-resistant strains even when the antibiotic use stops.)

Hmm, the antibiotic resistance article is exactly what I asked for. I imagine it's flawed in its methodology somehow, since the study was done by the Antimicrobial Chemotherapy lobby, but until I can figure out how, you win this particular point. However...

EDIT: Perhaps the resistant forms also provide a resistance to something else found in the pig's system? Hence, increased survival advantage even when the specific antiobiotic / antibody being tested for isn't present._________________Homeschool Articles - Events - Support Groups

Hmm, the antibiotic resistance article is exactly what I asked for. I imagine it's flawed in its methodology somehow, since the study was done by the Antimicrobial Chemotherapy lobby, but until I can figure out how, you win this particular point. However...

"The antimicrobial chemotherapy lobby"??? It is the name of the journal that the study was published in...the Journal of Antimicrobial Chemotherapy. That means it is a journal that publishes scientific papers dealing with antibiotics. Who is this lobby? What do you think their ulterior motives are? They are investigating the problems in treating infections of antibiotic resistant bacteria. They would include MD-PhDs, veterinary-PhDs, microbiologists, pathologists, etc.

That paper involved E. coli. I also posted information about M. tuberculosis. These are two examples that refute your claims about antibiotic resistant bacteria. I could send more.

What do you mean "is this an appropriate example of evolutionary change?" (paraphrased) Of course it is! Why wouldn't it be? It involves mutations that provide advantages to some individuals in a population under certain conditions. That is natural selection at work.

Last edited by knobren on Fri Jul 27, 2007 7:01 pm; edited 1 time in total

EDIT: Perhaps the resistant forms also provide a resistance to something else found in the pig's system? Hence, increased survival advantage even when the specific antiobiotic / antibody being tested for isn't present.

Antibiotics are chemicals that we take to slow the growth/reproduction of or to kill bacteria. Antibiotics are made by certain kinds of bacteria and fungi to slow the competition for nutrients, but we either purify them or make synthetic versions of them to use as drugs.

Different antibiotics affect different parts of bacterial cells. Some affect protein production, some affect cell wall production, etc. There are different ways that bacteria can become resistant to antibiotics, depending on the type of antibiotic. In the case of penicillin resistance, there are two ways for bacteria to overcome the penicillin. The most common way is to make an enzyme that digests the penicillin, so it can't interfere with cell wall production. The other way is to have mutations in the target of the penicillin, so it can't bind to and interfere with cell wall production. Resistance to other types of antibiotics can also involve alterations in the target of the antibiotic (i.e. RNA polymerase or ribosome) or production of an enzyme that degrades the antibiotic before it can bind to its target. Other types of resistance involve the active pumping of the antibiotic out of the cell (a dilution effect) and changes in the cell envelope that limits entry of the antibiotic in the first place.

Antibodies are proteins made by our immune systems to fight off foreign invaders. Bacteria have to evade those too, but that is a different discussion.

Microbiologists have known for some time that bacteria don't act the same way in culture that they do in the host organism. Pathogens that have been passed through cultures often lose some of their abilities to infect a host and evade host defenses. Different proteins are turned on/off in culture compared to inside the host. The nutrients are different; there isn't an active immune system; etc. That is one reason that comparing growth rates of resistant and non-resistant bacteria in lab cultures could give different results than they would in a competition inside a host animal. Also, some of the changes that make the bacteria resistant to the antibiotic in question are not specific to that particular antibiotic and could alter the way other substances are adsorbed, absorbed, etc. You supposed that this could be the case in your argument. However, what would that matter? ...the mutation is still beneficial to the bacteria, which is what we are discussing.

By "Antimicrobial Chemotherapy lobby", I just mean that they are obviously going to be in favor of antibiotic use, and an experiment that shows that bacteria don't easily lose their resistance in animals means that reducing antiobiotic use won't get rid of the resistant strains, and that new antibiotics are even more necessary. There will be bias, though whether or not that seriously impacts their science, I do not know. It all depends on where their funding comes from.

In any case, even if I give you this point, the article I linked to brings up an interesting question - if the bacteria are just "evolving" by acquiring genes that are already in existence, rather than creating new ones, then how can this be proof for macroevolution? You can shuffle a deck of cards all you want, and you'll never draw a 14 of Truffles. Also, this was animal testing on single animals, not animal testing on populations, and the bacteria also have to show a survival advantage for the host, since if the host dies, so do the bacteria. Weaponized biological agents do not survive long in real life, since the host dies at a much greater rate. 10 or 20 iterations at most and the large majority of their effectiveness is gone (albeit, having killed millions by then). A stronger bacteria won't necessarily survive longer than a weaker one._________________Homeschool Articles - Events - Support Groups

I can't seem to understand these articles you keep posting. Can you explain to me examples of how a creature can change into something of a different kind? Macroevolution._________________Phi 4:13 I can do all things through Christ which strengtheneth me.

By "Antimicrobial Chemotherapy lobby", I just mean that they are obviously going to be in favor of antibiotic use, and an experiment that shows that bacteria don't easily lose their resistance in animals means that reducing antiobiotic use won't get rid of the resistant strains, and that new antibiotics are even more necessary. There will be bias, though whether or not that seriously impacts their science, I do not know. It all depends on where their funding comes from.

In any case, even if I give you this point, the article I linked to brings up an interesting question - if the bacteria are just "evolving" by acquiring genes that are already in existence, rather than creating new ones, then how can this be proof for macroevolution? You can shuffle a deck of cards all you want, and you'll never draw a 14 of Truffles. Also, this was animal testing on single animals, not animal testing on populations, and the bacteria also have to show a survival advantage for the host, since if the host dies, so do the bacteria. Weaponized biological agents do not survive long in real life, since the host dies at a much greater rate. 10 or 20 iterations at most and the large majority of their effectiveness is gone (albeit, having killed millions by then). A stronger bacteria won't necessarily survive longer than a weaker one.

Good Grief! You think that antibiotic resistant bacteria are all a big hype dreamed up by drug companies and for-profit hospitals?????

Bacteria can pass genes to one another on plasmids, but that is not the only way that they can become resistant to drugs. Some mutations arise spontaneously in chromosomal genes.

When infectious organisms switch to new hosts, there is often a period where the organism is at its deadliest. Those pathogens that kill off their hosts before they have a chance to pass on the infection to more hosts will be selected against, so eventually, the infectious agent becomes less deadly. Also, those host organisms that are able to withstand the infection will be selected for and pass on their traits to the next generation. This is coevolution between host and pathogen.

"With the report in 1985 (3) of a community-based outbreak of penicillin-resistant gonorrhea due to a strain not producing a beta-lactamase, the final blow to penicillin therapy for treatment of this sexually transmitted infection was, unfortunately, realized. The culprit strain (FA6140 [3]) from this outbreak contained (12) a number of chromosomal mutations (penA, penB, ponA, and mtr) that are known to alter cell envelope structure and/or function. In general terms, these mutations impact penicillin's accumulation in gonococci (penB and mtr) or affinity (penA and ponA) for penicillin-binding proteins; this commentary will be restricted to issues related to penB and mtr. The penB mutation was originally linked (7) to production of an altered major outer membrane protein (termed POMP or protein I) and was found to confer two- to fourfold increases in MIC levels of penicillin and tetracycline. Curiously, phenotypic expression of penB required the presence of the mtr mutation, which was found to confer single-step resistance to structurally diverse hydrophobic antimicrobial agents (10) and was presumed to decrease cell envelope permeability to such agents (6). "

This is an amazing example of two different views from the same evidence. Creationists will automatically thinking Cain and Abel's descendants. I'm not sure what evolutionists are thinking. That is why I bring it up._________________Phi 4:13 I can do all things through Christ which strengtheneth me.

This is an amazing example of two different views from the same evidence. Creationists will automatically thinking Cain and Abel's descendants. I'm not sure what evolutionists are thinking. That is why I bring it up.

The human family tree is quite bushy and which hominids are our ancestors and which are our cousins have long been in dispute. This new evidence suggests that Homo habilis and Homo erectus may have lived during the same time period. This new evidence suggests that they may have been "cousins" instead of H. habilis being an ancestor of H. erectus. This new information lead to a reassessment of the fossils that were found previously. This is how science works. New data leads to reassessment and refinement of explanations.

That's how science is supposed to work, anyhow. It's been known for some time that you can get thicker jaws and even different jaw structures from eating a coarse diet, and arthritis can give the rounded, hunched skeletons normally associated with "missing links". The only difference between "ancient man" and "modern man" is the supposed age of the skeletons. There are natives living now in various parts of the world whose skeletons are indistinguishable from those of "ancient man", so are we to assume that they are lower forms of humanity and that we are higher forms? Evolution leads inescapably to racism.

Also, as I stated elsewhere, there are known cases of scientists actually dislocating the jaws of their skeletons so they can make them jut an inch or two more for photos. The skeletons may be real, but the photos are complete frabrications, and anyone who looks at the original skulls can easily see that they're identical to modern skulls. Regardless of whether you believe in evolution or not, stuff like this needs to stop. It makes science into a mockery and a fraud, though I suppose it's good snake oil for the masses._________________Homeschool Articles - Events - Support Groups

Joined: 04 Jul 2007Posts: 231Location: Standing in the radiance of His glory.

Posted: Mon Aug 20, 2007 5:11 am Post subject:

As I have said before, I will not argue the finer points of creationism vs. evolution, but I will point out how the minds of scientists work to fit everything into the evolution model, which can lead to erroneous conclusions.

I just watched a documentary about scientist retrieving a complete mammoth frozen in ice. The position of the mammoth, they agreed, suggested that the mammoth was in a pool of water when it froze. As they were carefully digging around it to free it from the surrounding ice, they found frozen vegetation, still green.

Then they said because of the depth of the aquatic vegetation they concluded it was thousands of years older than the mammoth. Now, it was just a foot or two under the mammoth's feet, so why is it assumed because it is under the mammoth that it is older rather than it was at the bottom of the pool when the mammoth froze? Would it be because scientists are programmed to think depth means age? I mean, I would imagine that a mammoth struggling to get out of the water would have stirred up the mud at the bottom of a pond, right?

I still cannot get around that, even if I did believe in evolution. Here is a mammoth swimming, according to the positioning of its body, and it gets frozen in ice. Maybe fell through the ice and was struggling to get out, but the scientists stated that the mammoths lived there, in Siberia, at a time when it was green--not covered with ice. So, they assume it when into the water and got stuck in the mud. Okay, but what about the green plant? If it was layers down from the mammoth buried in mud, instead of ice when the mammoth entered the pond, why would it be still green?

Sometimes scientists are so eager to prove their theories based on the evolutionary model that they don't see how the facts don't fit--they simply must fit so they make theories to make them fit. Circular reasoning.